How to Measure Arterial Stiffness in Humans Segers, Patrick; Rietzschel, Ernst R; Chirinos, Julio A
Arteriosclerosis, thrombosis, and vascular biology
40, Issue:
5
Journal Article
Peer reviewed
Open access
Despite the wide recognition of larger artery stiffness as a highly clinically relevant and independent prognostic biomarker, it has yet be incorporated into routine clinical practice and to take a ...more prominent position in clinical guidelines. An important reason may be the plethora of methods and devices claiming to measure arterial stiffness in humans. This brief review provides a concise overview of methods in use, indicating strengths and weaknesses. We classified and graded methods, highly weighing their scrutiny and purity in quantifying arterial stiffness, rather than focusing on their ease of application or the level at which methods have demonstrated their prognostic and diagnostic potential.
Previous research has shown that nutrients and certain food items influence inflammation. However, little is known about the associations between diet, as a whole, and inflammatory markers. In the ...present study, we examined the ability of a FFQ-derived dietary inflammatory index (DII) to predict inflammation. Data from a Belgian cross-sectional study of 2524 generally healthy subjects (age 35–55 years) were used. The DII is a population-based, literature-derived dietary index that was developed to predict inflammation and inflammation-related chronic diseases. The DII was calculated from FFQ-derived dietary information and tested against inflammatory markers, namely C-reactive protein (CRP), IL-6, homocysteine and fibrinogen. Analyses were performed using multivariable logistic regression, adjusting for energy, age, sex, BMI, smoking status, education level, use of non-steroidal anti-inflammatory drugs, blood pressure, use of oral contraceptives, anti-hypertensive therapy, lipid-lowering drugs and physical activity. Multivariable analyses showed significant positive associations between the DII and the inflammatory markers IL-6 (>1·6 pg/ml) (OR 1·19, 95 % CI 1·04, 1·36) and homocysteine (>15 μmol/l) (OR 1·56, 95 % CI 1·25, 1·94). No significant associations were observed between the DII and the inflammatory markers CRP and fibrinogen. These results reinforce the fact that diet, as a whole, plays an important role in modifying inflammation.
The rapid technological developments of the past decade and the changes in echocardiographic practice brought about by these developments have resulted in the need for updated recommendations to the ...previously published guidelines for cardiac chamber quantification, which was the goal of the joint writing group assembled by the American Society of Echocardiography and the European Association of Cardiovascular Imaging. This document provides updated normal values for all four cardiac chambers, including three-dimensional echocardiography and myocardial deformation, when possible, on the basis of considerably larger numbers of normal subjects, compiled from multiple databases. In addition, this document attempts to eliminate several minor discrepancies that existed between previously published guidelines.
The rapid technological developments of the past decade and the changes in echocardiographic practice brought about by these developments have resulted in the need for updated recommendations to the ...previously published guidelines for cardiac chamber quantification, which was the goal of the joint writing group assembled by the American Society of Echocardiography and the European Association of Cardiovascular Imaging. This document provides updated normal values for all four cardiac chambers, including three-dimensional echocardiography and myocardial deformation, when possible, on the basis of considerably larger numbers of normal subjects, compiled from multiple databases. In addition, this document attempts to eliminate several minor discrepancies that existed between previously published guidelines.
The aim of the Lancet Commission on hypertension is to identify key actions to improve the management of blood pressure both at the population and the individual level, and to generate a campaign to ...adopt the suggested actions at national levels to reduce the impact of elevated blood pressure globally. The first task of the Commission is this report, which briefly reviews the available evidence for prevention, identification, and treatment of elevated blood pressure, hypertension, and its cardiovascular complications.
Full text
Available for:
GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK, ZRSKP
Telomeres shorten with age, the major risk factor for atherosclerotic cardiovascular disease (aCVD). The observation of shorter telomeres in aCVD patients thus suggested that critical telomere ...shortening may contribute to premature biological aging and aCVD. Therefore, telomere length often is suggested as a causal aCVD risk factor, a proposal supported by recent Mendelian randomization studies; however, epidemiological research has shown disappointingly low effect sizes. It therefore remains uncertain whether telomere shortening is a cause of aCVD or merely a consequence. The authors argue that elucidating the mechanistic foundation of these findings is essential for any possible translation of telomere biology to the clinic. Here, they critically evaluate evidence for causality in animal models and human studies, and review popular hypotheses and discuss their clinical implications. The authors identify 4 key questions that any successful mechanistic theory should address, and they discuss how atherosclerosis-associated local telomere attrition may provide the answers.
Full text
Available for:
GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
The impact of increased serum concentrations of plant sterols on cardiovascular risk is unclear. We conducted a systematic review and meta-analysis aimed to investigate whether there is an ...association between serum concentrations of two common plant sterols (sitosterol, campesterol) and cardiovascular disease (CVD). We systematically searched the databases MEDLINE, EMBASE, and COCHRANE for studies published between January 1950 and April 2010 that reported either risk ratios (RR) of CVD in relation to serum sterol concentrations (either absolute or expressed as ratios relative to total cholesterol) or serum sterol concentrations in CVD cases and controls separately. We conducted two meta-analyses, one based on RR of CVD contrasting the upper vs. the lower third of the sterol distribution, and another based on standardized mean differences between CVD cases and controls. Summary estimates were derived by fixed and random effects meta-analysis techniques. We identified 17 studies using different designs (four case-control, five nested case-control, three cohort, five cross-sectional) involving 11 182 participants. Eight studies reported RR of CVD and 15 studies reported serum concentrations in CVD cases and controls. Funnel plots showed evidence for publication bias indicating small unpublished studies with non-significant findings. Neither of our meta-analyses suggested any relationship between serum concentrations of sitosterol and campesterol (both absolute concentrations and ratios to cholesterol) and risk of CVD. Our systematic review and meta-analysis did not reveal any evidence of an association between serum concentrations of plant sterols and risk of CVD.
Diastolic dysfunction is considered the first marker of diabetic cardiomyopathy. However, preclinical systolic alteration was also recently described by strain, but its association with diastolic ...dysfunction has never been investigated.
One hundred fourteen patients with type 2 diabetes mellitus (DM) with controlled blood pressure and without overt heart disease were prospectively enrolled and compared with 88 age-matched controls. All subjects underwent comprehensive echocardiography, including diastolic evaluation according to current recommendations and speckle-tracking imaging. The prevalence of diastolic dysfunction, the determinants of diastolic parameters, and the association between preclinical systolic and diastolic dysfunctions were studied.
Diastolic parameters were altered in patients compared with controls, with lower E/A ratios, longer mitral deceleration and isovolumic relaxation times, and higher E/e' ratio. Diastolic dysfunction occurred in 47% of patients with DM (33% and 14% with grade I and II diastolic dysfunction, respectively) and systolic alteration (longitudinal strain ≥ -18%) in 32% of patients. Whereas longitudinal systolic strain was independently associated with DM and gender, diastolic parameters were influenced by many factors, including age, rate-pressure product, history of hypertension, and body mass index. Systolic alteration occurred in 28% of patients with DM with normal diastolic function and in 35% with diastolic dysfunction.
Diastolic dysfunction diagnosed according to current recommendations is frequent in patients with DM but is also influenced by other factors. Systolic strain alteration may exist despite normal diastolic function, indicating that diastolic dysfunction should not be considered the first marker of a preclinical form of diabetic cardiomyopathy.
Obesity increases the risk of heart failure and atrial fibrillation. Left atrial (LA) dysfunction is increasingly recognized as a mediator of cardiovascular disease. Early effects of obesity on LA ...function have not been examined in large population samples. We quantified LA strain and strain rate (SR) through speckle tracking echocardiography in 1,531 middle-aged community-based participants enrolled in the Asklepios study. We compared LA function between individuals with body mass index (BMI) < 25 kg/m2 (n = 779), 25 to 29.9 kg/m2 (n = 618) and ≥ 30 kg/m2 (n = 134). Significant differences in reservoir longitudinal LA strain (BMI < 25 kg/m2 = 35.3%, BMI 25–29.9 kg/m2 = 33.1%, and BMI ≥ 30 kg/m2 = 30.9%; p < 0.00001) strain rate (SR BMI < 25 kg/m2 = 151; BMI 25 to 29.9 kg/m2 = 141; and BMI ≥ 30 kg/m2 = 135 %/s; p <0.00001) and expansion index (BMI < 25 kg/m2 = 1.6, BMI 25 to 29.9 kg/m2 = 1.4, and BMI ≥ 30 kg/m2 = 1.4; p <0.00001) were seen, indicating reduced reservoir function with increasing BMI. Obesity was also associated with impaired LA conduit function, including conduit longitudinal LA strain (BMI < 25 kg/m2 = 21.6%, BMI 25 to 29.9 kg/m2 = 18.9%, and BMI ≥ 30 kg/m2 = 16.7%; p <0.00001), SR (BMI < 25 kg/m2 = −189, BMI 25 to 29.9 kg/m2 = 166, and BMI ≥ 30 kg/m2 = 150 %/s; p <0.0001) and passive LA emptying fraction (BMI < 25 kg/m2 = 40.5, BMI 25 to 29.9 kg/m2 = 36.5, and BMI ≥ 30 kg/m2 = 36%, p <0.00001). These differences persisted after adjustment for age, gender and other potential confounders. In contrast to reservoir and conduit function, obesity was associated with increased booster pump function (active LA emptying fraction: BMI < 25 kg/m2 = 19.4%, BMI 25 to 29.9 kg/m2 = 20.5%, and BMI ≥ 30 kg/m2 = 21.5%; p <0.00001). In middle-aged adults, obesity is associated with impaired reservoir and conduit LA function and higher booster function, which may be compensatory. Loss of booster LA function, either because of more advanced LA dysfunction or atrial fibrillation, may play an important role in precipitating heart failure in obese individuals.
Full text
Available for:
GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
PDF
